Common misconceptions

Common mistake
Wrong: PMR causes elevated CK and muscle enzyme levels like inflammatory myopathies.
Right: PMR causes markedly elevated ESR and CRP but normal CK and muscle enzymes, distinguishing it from true myositis.
PMR causes inflammation around joints and bursae — it does not damage muscle fibers themselves, so CK and aldolase remain normal. Elevated CK is the hallmark of true myositis (like polymyositis or dermatomyositis), where muscle cells are being destroyed. In PMR, the labs you'll see are a dramatically elevated ESR (often >50–100 mm/hr) and CRP with completely normal muscle enzymes. If a vignette gives you proximal weakness with elevated CK, think myositis — not PMR.
Common mistake
Wrong: PMR and GCA are treated with the same dose of prednisone.
Right: PMR is treated with low-dose prednisone (~15–20 mg/day), while GCA requires high-dose prednisone (40–60 mg/day) to prevent irreversible vision loss.
The dose difference isn't arbitrary — it reflects the severity of what each condition can do. PMR, while painful, doesn't cause end-organ damage at low steroid doses. GCA threatens the ophthalmic artery, and if left undertreated, causes permanent vision loss within hours to days. High-dose prednisone (40–60 mg/day) is needed to suppress the large-vessel granulomatous inflammation fast enough to protect the eye. Giving a PMR-level dose to a GCA patient is a dangerous mistake that the exam explicitly tests.
Common mistake
Gap: Misses that steroids should not be delayed pending temporal artery biopsy when GCA is suspected
When GCA is suspected alongside PMR, high-dose steroids must be started immediately before temporal artery biopsy to prevent vision loss; biopsy can still be positive for up to 2 weeks after steroid initiation.
The biopsy confirms the diagnosis but does not guide the initial treatment decision when vision is at risk. Steroids must be started immediately if GCA is clinically suspected — waiting for biopsy results is not acceptable. The key fact to memorize: temporal artery biopsy remains positive for up to 2 weeks after steroid initiation because granulomatous changes persist even as active inflammation is suppressed. So you never have to choose between treating and diagnosing — start steroids, then get the biopsy within the week.
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What the exam tests

  1. Recognize the classic PMR presentation: bilateral proximal muscle stiffness (shoulders and hips) in a patient over 50, with markedly elevated ESR/CRP but normal CK and muscle enzymes — and distinguish it from true inflammatory myopathies like polymyositis.
  2. Identify features that suggest concurrent GCA in a PMR patient (new headache, jaw claudication, vision changes, temporal artery tenderness) and know that this is an emergency requiring immediate high-dose steroids, not a workup-first situation.
  3. Apply the correct steroid dosing for each condition: low-dose prednisone for isolated PMR (~15–20 mg/day) versus high-dose prednisone for GCA (40–60 mg/day), and understand why the difference exists — vision loss prevention.

Can you avoid these mistakes?

A 72-year-old woman presents with 3 months of bilateral shoulder and hip stiffness, worst in the morning and lasting over an hour. ESR is 85 mm/hr, CRP is elevated, CK is normal. What is the diagnosis, and what finding would most change your management approach?
You start a 68-year-old man on prednisone 20 mg/day for PMR. Two weeks later he returns with a new unilateral headache, jaw pain when chewing, and blurry vision in one eye. What is the next best step — and what dose of prednisone should he receive?
How do you distinguish PMR from polymyositis on labs alone? List the key findings you'd expect in each condition for ESR, CRP, and CK.
A patient with suspected GCA is scheduled for temporal artery biopsy tomorrow. A medical student suggests waiting to start steroids until after the biopsy to avoid affecting the results. Is this correct? What is the maximum time steroids can be given before a biopsy still yields a useful result?

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